ArticleInfection and immunity2009
Shiga toxin 2 targets the murine renal collecting duct epithelium.
Article in Infection and immunity, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
48 citing papers in PubMed, 83 citations in OpenAlex.
- Redefining Shiga toxin-induced human cell death as NLRP1- and gasdermin E-mediated pyroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Pathogenesis and therapeutic strategies in the interaction between gut microbiota and enterohemorrhagic Escherichia coli infection.FEMS microbiology reviews · 2026Review
- Eliglustat prevents acute kidney injury caused by Shiga toxin 2 in lethal and sublethal rat models of hemolytic uremic syndrome.Frontiers in pharmacology · 2026Article
- Advanced Three-Dimensional Cell Culture Models for Investigating EnterohaemorrhagicJournal of microbiology and biotechnology · 2025Review
- EnterohemorrhagicFrontiers in cellular and infection microbiology · 2025Article
- Extracellular DNA concentrations in various aetiologies of acute kidney injury.Scientific reports · 2022Article
- Eliglustat prevents Shiga toxin 2 cytotoxic effects in human renal tubular epithelial cells.Pediatric research · 2022Article
- Citrobacter rodentium(ϕStx2dact), a murine infection model for enterohemorrhagic Escherichia coli.Current opinion in microbiology · 2022Review
- Stx2 Induces Differential Gene Expression and Disturbs Circadian Rhythm Genes in the Proximal Tubule.Toxins · 2022Article
- Role of Globotriaosylceramide in Physiology and Pathology.Frontiers in molecular biosciences · 2022Review
- Cell Biological Responses after Shiga Toxin-1 Exposure to Primary Human Glomerular Microvascular Endothelial Cells from Pediatric and Adult Origin.International journal of molecular sciences · 2021Article
- Shiga Toxin-Bearing Microvesicles Exert a Cytotoxic Effect on Recipient Cells Only When the Cells Express the Toxin Receptor.Frontiers in cellular and infection microbiology · 2020Article
- Molecular stratification of idiopathic nephrotic syndrome.Nature reviews. Nephrology · 2019Review
- Structural Insights intoMicroorganisms · 2019Article
- Medullary thick ascending limb impairment in the GlaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Exosome-associated Shiga toxin 2 is released from cells and causes severe toxicity in mice.Scientific reports · 2018Article
- Advances in our understanding of the pathogenesis of hemolytic uremic syndromes.American journal of physiology. Renal physiology · 2018Review
- Modeling Hemolytic-Uremic Syndrome: In-Depth Characterization of Distinct Murine Models Reflecting Different Features of Human Disease.Frontiers in immunology · 2018Article
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Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Hemolytic-uremic syndrome (HUS) caused by Shiga toxin-producing Escherichia coli infection is a leading cause of pediatric acute renal failure. Bacterial toxins produced in the gut enter the circulation and cause a systemic toxemia and targeted cell damage. It had been previously shown that injection of Shiga toxin 2 (Stx2) and lipopolysaccharide (LPS) caused signs and symptoms of HUS in mice, but the mechanism leading to renal failure remained uncharacterized. The current study elucidated that murine cells of the glomerular filtration barrier were unresponsive to Stx2 because they lacked the receptor glycosphingolipid globotriaosylceramide (Gb(3)) in vitro and in vivo. In contrast to the analogous human cells, Stx2 did not alter inflammatory kinase activity, cytokine release, or cell viability of the murine glomerular cells. However, murine renal cortical and medullary tubular cells expressed Gb(3) and responded to Stx2 by undergoing apoptosis. Stx2-induced loss of functioning collecting ducts in vivo caused production of increased dilute urine, resulted in dehydration, and contributed to renal failure. Stx2-mediated renal dysfunction was ameliorated by administration of the nonselective caspase inhibitor Q-VD-OPH in vivo. Stx2 therefore targets the murine collecting duct, and this Stx2-induced injury can be blocked by inhibitors of apoptosis in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.